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  • Open Access

    ARTICLE

    Analysis and Verification of the Conserved MYB Binding Element in the DFR Promoter in Compositae

    Jialei Guo1,2, Fengzhen Li2, Guomin Shi3, Weimin Zhao2, Tao He1,2,*

    Phyton-International Journal of Experimental Botany, Vol.93, No.2, pp. 343-353, 2024, DOI:10.32604/phyton.2024.047429

    Abstract Anthocyanins, ubiquitous in the Compositae family, are regulated by MYB (v-myb avian myeloblastosis viral oncogene homolog), playing an important role in anthocyanin synthesis. In this study, we analyzed the regulation pathway in which the MYB protein of subgroup 6 promotes dihydroflavonol reductase (DFR) expression in Compositae, and validated this law in Saussurea medusa through yeast one-hybrid experiments. Our results showed that MYB and DFR underwent purification selection, DFR promoter analysis revealed the presence of MYB binding site (GAGTTGAATGG) and bHLH binding site (CANNTG) at the sense strand of 84–116 nucleotide residues from the start codon. These two motifs were separated… More >

  • Open Access

    ARTICLE

    Cloning of and analysis of cadmium resistant in Potentilla sericea

    ZHENGHONG FENG1, BING GAO1, YU GAO2, JIANHUI WU1,*

    BIOCELL, Vol.47, No.7, pp. 1571-1582, 2023, DOI:10.32604/biocell.2023.029106

    Abstract Background:Potentilla sericea is a heavy metal hyperaccumulator landscaping plant. MYB transcription factors play an important role in regulating plant stress response to adversity. However, there are few studies on MYB transcription factors in stress tolerance in Potentilla sericea. In this study, the gene was successfully cloned from Potentilla sericea. Methods: Bioinformatic analysis and real-time quantitative PCR (qPCR) methods were used to evaluate this gene. The transgenic A. thaliana were obtained by flower dipping and the gene function was identified by determining physiological indicators under cadmium stress. Results: The open reading frame of is 942 bp, which encodes 313 amino acids… More >

  • Open Access

    ARTICLE

    miR-150 Suppresses Tumor Growth in Melanoma Through Downregulation of MYB

    Xiyan Sun*1, Chao Zhang†1, Yang Cao, Erbiao Liu*

    Oncology Research, Vol.27, No.3, pp. 317-323, 2019, DOI:10.3727/096504018X15228863026239

    Abstract miR-150 has been demonstrated to inhibit tumor progression in various human cancers, including colorectal cancer, ovarian cancer, and thyroid cancer. However, the role of miR-150 in melanoma remains to be determined. In this study, we found that miR-150 was underexpressed in melanoma tissues and cell lines. Through transfection of miR-150 mimics, we found that miR-150 significantly inhibited the proliferation, migration, and invasion of melanoma cells. In mechanism, we found that MYB was a target of miR-150 in melanoma cells. Overexpression of miR-150 significantly inhibited mRNA and protein levels of MYB in melanoma cells. Moreover, there was an inverse correlation between… More >

  • Open Access

    ARTICLE

    The BHLH Transcriptional Factor PIF4 Competes with the R2R3-MYB Transcriptional Factor MYB75 to Fine-Tune Seeds Germination under High Glucose Stress

    Xiaoli Li, Shiyan Lu, Yaru Yang, Wenjie Wei, Jiali Wei, Xiaojun Yuan*, Ping Li*

    Phyton-International Journal of Experimental Botany, Vol.90, No.5, pp. 1387-1400, 2021, DOI:10.32604/phyton.2021.016362

    Abstract It is known that the high level of sugar including glucose suppresses seed germination through ABA signal. ABI5 is an essential component to mediate ABA-dependent seed germination inhibition, but underlying mechanism needs more investigation. Previous study demonstrated the PIF4 activated the expression of ABI5 to suppress seed germination in darkness. Here we reported that PIF4 also mediated the seed germination inhibition through ABI5 under high concentration of glucose treatment. Furthermore, we found that PIF4 interacted with PAP1, the central factor to control anthocyanin biosynthesis. Such interaction was confirmed in vitro and in planta. Biochemical and physiological analysis revealed that PAP1… More >

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